199 research outputs found
Hypovitaminosis D in developing countries-prevalence, risk factors and outcomes
No full textHypovitaminosis D is a prevalent disorder in developing countries. Clinical manifestations of hypovitaminosis D include musculoskeletal disorders, such as nonspecific muscle pain, poor muscle strength and low BMD, as well as nonmusculoskeletal disorders, such as an increased risk of respiratory infections, diabetes mellitus and possibly cardiovascular diseases. In developing countries, the prevalence of hypovitaminosis D varies widely by and within regions; prevalence ranges between 30-90percent, according to the cut-off value used within specific regions, and is independent of latitude. A high prevalence of the disorder exists in China and Mongolia, especially in children, of whom up to 50percent are reported to have serum 25-hydroxyvitamin D levels 12.5 nmol-l. Despite ample sunshine throughout the year, one-third to one-half of individuals living in Sub-Saharan Africa and the Middle East have serum 25-hydroxyvitamin D levels 25 nmol-l, according to studies published in the past decade. Hypovitaminosis D is also prevalent in children and the elderly living in Latin America. Risk factors for hypovitaminosis D in developing countries are similar to those reported in Western countries and include extremes of age, female sex, winter season, dark skin pigmentation, malnutrition, lack of sun exposure, a covered clothing style and obesity. Clinical trials to assess the effect of vitamin D supplementation on classical and nonclassical clinical outcomes in developing countries are needed. © 2010 Macmillan Publishers Limited. 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PTH level but not 25 (OH) vitamin D level predicts bone loss rates in the elderly
No full textWe assessed the impact of calciotropic hormones on bone loss in 195 elderly subjects. After a median follow up of 4 years, parathyroid hormone (PTH) correlated negatively with changes in bone mineral density (BMD) at all skeletal sites. After adjustment for potential predictors of bone loss in the elderly, PTH level alone explained 3percent of the variance in BMD changes at the hip. Introduction: This study assessed the impact of calciotropic hormones on bone loss rates in an elderly population-based cohort of 195 ambulatory men and women, aged 65-85 years and followed up for a median of 4 years. Methods: Calcium intake, serum calcium, and phosphorus were assessed at baseline. Serum creatinine was measured at follow up visit. The 25 (OH) vitamin D [25-OHD] and PTH were measured at baseline and at follow up. Bone mass at the lumbar spine, hip, forearm and total body, as well as body composition was measured at baseline and at follow up by dual energy X-ray absorptiometry. Results: Mean 25-OHD level was 14.7 ± 6.4 ng-ml and mean PTH level was 47.9 ± 30.4 pg-ml. Age correlated negatively with percent changes in BMD at all skeletal sites (p 0.05). Changes in body mass index (BMI) and in body composition correlated positively with BMD changes at all sites, except at the forearm. There was no correlation between 25-OHD and changes in BMD except at the trochanter (r = 0.19, p 0.008). Conversely, PTH negatively correlated with changes in BMD at all skeletal sites (r = -0.14 to -0.27, p 0.05). This correlation persisted after adjustment for age, changes in BMI, changes in fat mass and lean mass, serum creatinine, calcium intake, and 25-OHD levels. PTH level alone explained 3percent of the variance in BMD changes at all hip subregions. Conclusions: Serum PTH, but not 25-OHD, predicted bone loss rates in the elderly. Thus, it is important to normalize PTH level when correcting hypovitaminosis D in the elderly. © 2011 International Osteoporosis Foundation and National Osteoporosis Foundation.Adami S, 2009, OSTEOPOROSIS INT, V20, P239, DOI 10.1007-s00198-008-0650-y; Arabi A, 2006, BONE, V39, P268, DOI 10.1016-j.bone.2006.01.140; Baddoura R, 2007, BONE, V40, P1066, DOI 10.1016-j.bone.2006.11.016; Bischoff-Ferrari HA, 2005, JAMA-J AM MED ASSOC, V293, P2257, DOI 10.1001-jama.293.18.2257; Bischoff-Ferrari HA, 2004, JAMA-J AM MED ASSOC, V291, P1999, DOI 10.1001-jama.291.16.1999; Bischoff-Ferrari HA, 2004, AM J MED, V116, P634, DOI 10.1016-j.amjmed.2003.12.029; Bjornerem A, 2007, CALCIFIED TISSUE INT, V81, P65, DOI 10.1007-s00223-007-9035-z; Blain H, 2004, J GERONTOL A-BIOL, V59, P1285; Boonen S, 2007, J CLIN ENDOCR METAB, V92, P1415, DOI 10.1210-jc.2006-1404; Collins D, 1998, OSTEOPOROSIS INT, V8, P110, DOI 10.1007-BF02672505; Deane A, 2007, BMC MUSCULOSKEL DIS, V8, DOI 10.1186-1471-2474-8-3; Dennison E, 1999, OSTEOPOROSIS INT, V10, P384, DOI 10.1007-s001980050244; Emaus N, 2006, AM J EPIDEMIOL, V163, P441, DOI 10.1093-aje-kwj055; Ensrud KE, 2009, J CLIN ENDOCR METAB, V94, P2773, DOI 10.1210-jc.2008-2786; Fradinger EE, 2001, OSTEOPOROSIS INT, V12, P24, DOI 10.1007-s001980170153; Garnero P, 2007, BONE, V40, P716, DOI 10.1016-j.bone.2006.09.026; Gennari L, 2003, J CLIN ENDOCR METAB, V88, P5327, DOI 10.1210-jc.2003-030736; Hannan MT, 2000, J BONE MINER RES, V15, P710, DOI 10.1359-jbmr.2000.15.4.710; Ho-Pham LT, 2010, BMC MUSCULOSKEL DIS, V26, P59; KROLNER B, 1982, ACTA RADIOL DIAGN, V23, P517; Kuchuk NO, 2007, CLIN ENDOCRINOL, V67, P295, DOI 10.1111-j.1365-2265.2007.02882.x; Mellstrom D, 2008, J BONE MINER RES, V23, P1548; Mosekilde L, 2008, CLIN ENDOCRINOL, V69, P1, DOI 10.1111-j.1365-2265.2007.03162.x; Pottelbergh V, 2003, J CLIN ENDOCR METAB, V88, P075; Rand T, 1997, CALCIFIED TISSUE INT, V35, P667; Reid IR, 2008, OSTEOPOROSIS INT, V19, P595, DOI 10.1007-s00198-007-0492-z; RIGGS BL, 1986, NEW ENGL J MED, V314, P1676, DOI 10.1056-NEJM198606263142605; Sahota O, 2004, BONE, V35, P312, DOI 10.1016-j.bone.2004.02.003; Salamoun MM, 2005, EUR J CLIN NUTR, V59, P177, DOI 10.1038-sj.ejcn.1602056; Stewart KJ, 2005, AM J PREV MED, V28, P453, DOI 10.1016-j.amepre.2005.02.003; Stone K, 1998, J BONE MINER RES, V13, P1167, DOI 10.1359-jbmr.1998.13.7.1167; van Schoor NM, 2008, BONE, V42, P260, DOI 10.1016-j.bone.2007.11.002; Yoshimura N, 2011, J BONE MINER METAB, V29, P96, DOI 10.1007-s00774-010-0197-9; Zhai G, 2008, OSTEOPOROSIS INT, V19, P1211, DOI 10.1007-s00198-008-0562-x17141
Postprandial ghrelin and PYY responses of male subjects on low carbohydrate meals to varied balancing proportions of proteins and fats
No full textPurpose: This study was conducted to investigate whether a higher proportion of protein or fat is more favorable for optimal ghrelin and peptide YY (PYY) release in subjects consuming low carbohydrate meals. Methods: Eight normal weight men received, on three separate occasions, high protein low fat (HPLF) (40percent protein, 25percent fat), low protein high fat (LPHF) (10percent protein, 55percent fat) or medium protein medium fat (MPMF) (25percent protein, 40percent fat) meals, with equal low carbohydrates content in all three meals (35percent of energy). Postprandial blood samples were collected before and 15, 30, 60, 120, 180 and 240 min following the ingestion of each meal. Plasma acylated ghrelin and PYY 3-36 as well as serum insulin, glucose and triglycerides were measured. Results: Comparing meals and considering each time point separately, a trend for a statistically significant difference in acylated ghrelin was observed between HPLF and LPHF meals and a statistically significant change of PYY from baseline was noted between HPLF and LPHF meals as compared to the MPMF meal at certain time points. When data were pooled together, a statistically significant difference in acylated ghrelin change from baseline was observed between HPLF and LPHF meals, while both HPLF and LPHF meals resulted in a significantly higher PYY3-36 release in comparison to MPMF meal. AUC data analysis for PYY3-36 revealed significantly higher values following HPLF in comparison to MPMF meal. Correlation analysis revealed a significant negative correlation between acylated ghrelin and insulin only with the HPLF meal. Postprandial glucose and triglyceride levels were not significantly different between the three meals. 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Beta-thalassemia intermedia: An overview
No full text[No abstract available]Aessopos A, 2005, CHEST, V127, P1523, DOI 10.1378-chest.127.5.1523; Aessopos A, 2001, BLOOD, V97, P3411, DOI 10.1182-blood.V97.11.3411; CAPELLINI MD, 2002, HEMATOL J, V65; CAPELLINI MD, 2007, GUIDELINES CLIN MANA, pCH11; Cappellini MD, 2005, SEMIN HEMATOL, V42, pS19, DOI 10.1053-j.seminhematol.2005.01.001; Cappellini MD, 2000, BRIT J HAEMATOL, V111, P467, DOI 10.1046-j.1365-2141.2000.02376.x; Castelli R, 2004, AM J MED SCI, V328, P299, DOI 10.1097-00000441-200411000-00012; Chehal Aref, 2003, Spine (Phila Pa 1976), V28, pE245, DOI 10.1097-00007632-200307010-00024; Dixit A, 2005, ANN HEMATOL, V84, P441, DOI 10.1007-s00277-005-1026-4; Eldor A, 2002, BLOOD, V99, P36, DOI 10.1182-blood.V99.1.36; GIMMON Z, 1982, PLAST RECONSTR SURG, V69, P320, DOI 10.1097-00006534-198202000-00023; Karimi M, 2005, J PEDIAT HEMATOL ONC, V27, P380, DOI 10.1097-01.mph.0000174386.13109.28; Kushner J P, 2001, Hematology Am Soc Hematol Educ Program, P47; Mourad FH, 2003, BRIT J HAEMATOL, V121, P187, DOI 10.1046-j.1365-2141.2003.04240.x; Origa R, 2005, ANN NY ACAD SCI, V1054, P451, DOI 10.1196-annals.1345.051; PERRINE SP, 1993, NEW ENGL J MED, V328, P81, DOI 10.1056-NEJM199301143280202; St Pierre TG, 2005, BLOOD, V105, P855, DOI 10.1182-blood-2004-01-0177; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-0267; TAHER A, 2006, BLOOD CELL MOL DIS, V27, P12; TAHER A, 2007, ASH ANN M, V110, P3818; Weatherall DJ, 2001, J HEMATOL S1, V86, P18694
Hydrophilic interaction liquid chromatography-mass spectrometry for the characterization of glycoproteins at the glycan, peptide, subunit, and intact level
No full textThis chapter presents a methodical overview of recent research literature dealing with the characterization of glycoproteins by hydrophilic interaction chromatography separations coupled to mass spectrometry (HILIC-MS). This includes the analysis of intact glycosylated proteins as well as released glycans, glycopeptides, and protein subunits obtained after enzymatic digestion. The chapter provides basic background information on HILIC and glycoproteins, and the molecular levels at which glycosylation can be characterized. Next, essential HILIC parameters such as (the choice of) stationary phase type, mobile phase conditions, injection volume, and column temperature are reviewed. Herein focus is on the effect that these parameters have on both HILIC separation and MS detection. This is discussed in the context of the respective levels (glycan/peptide/subunit/intact) of glycoprotein analysis and current trends are highlighted. In the final part of this chapter, these developments are put in perspective by treating several applications of HILIC-MS for glycoprotein analysis in more detail, particularly in biopharmaceutical and clinical fields.</p
Effect of vitamin D replacement on hip structural geometry in adolescents: A randomized controlled trial
No full textBackground: We have shown in a randomized controlled trial that vitamin D increases bone mass, lean mass and bone area in adolescent girls, but not boys. These increments may translate into improvements in bone geometry and therefore bone strength. This study investigated the impact of vitamin D on hip geometric dimensions from DXA-derived hip structural analyses in adolescents who participated in the trial. Methods: 167 girls (mean age 13.1years) and 171 boys (mean age 12.7years) were randomly assigned to receive weekly placebo oil or vitamin D3, at doses of 1400IU or 14,000IU, in a double blind placebo-controlled 1-year trial. DXA images were obtained at baseline and one year, and hip images were analyzed using the hip structural analysis (HSA) software to derive parameters of bone geometry. These include outer diameter (OD), cross sectional area (CSA), section modulus (Z), and buckling ratio (BR) at the narrow neck (NN), intertrochanteric (IT), and shaft (S) regions. Analysis of Covariance (ANCOVA) was used to examine group differences for changes of bone structural parameters. Results: In the overall group of girls, vitamin D supplementation increased aBMD (7.9percent and 6.8percent in low and high doses, versus 4.2percent in placebo) and reduced the BR of NN (6.1percent and 2.4percent in low and high doses, versus 1.9percent in placebo). It also improved aBMD (7.9percent and 5.2percent versus 3.6percent) and CSA (7.5percent and 5.1percent versus 4.1percent) of the IT and OD of the S (2.4percent and 2.5percent versus 0.8percent respectively). Significant changes in the OD and BR of the NN, in the overall group of girls remained, after adjusting for lean mass, and were unaffected with further adjustments for lifestyle, pubertal status, and height measures. Conversely, boys did not exhibit any significant changes in any parameters of interest. A dose effect was not detected and subgroup analyses revealed no beneficial effect of vitamin D by pubertal stage. Conclusions: Vitamin D supplementation improved bone mass and several DXA-derived structural bone parameters, in adolescent girls, but not boys. This occurred at a critical site, the femoral neck, and if maintained through adulthood could improve bone strength and lower the risk of hip fractures. © 2013 Elsevier Inc.Abrams SA, 2011, CURR OPIN CLIN NUTR, V14, P605, DOI 10.1097-MCO.0b013e32834b2b01; Abrams SA, 2012, NUTR REV, V70, P201, DOI 10.1111-j.1753-4887.2012.00475.x; Arabi A, 2004, BONE, V35, P1169, DOI 10.1016-j.bone.2004.06.015; BECK TJ, 1992, CALCIFIED TISSUE INT, V50, P24, DOI 10.1007-BF00297293; BECK TJ, 1990, INVEST RADIOL, V25, P6, DOI 10.1097-00004424-199001000-00004; Beck TJ, 2002, HIP STRUCTURAL ANAL; Bischoff-Ferrari HA, 2012, RHEUM DIS CLIN N AM, V38, P107, DOI 10.1016-j.rdc.2012.03.010; Bischoff-Ferrari HA, 2012, NEW ENGL J MED, V367, P40, DOI 10.1056-NEJMoa1109617; Bonjour JP, 1996, OSTEOPOROSIS; Bueno AL, 2008, J PEDIAT, V84, P386, DOI [10.2223-JPED.1816, 10.1590-S0021-75572008000600003]; Burnham JM, 2007, J BONE MINER RES, V22, P551, DOI 10.1359-JBMR.070110; Ceglia L, 2008, MOL ASPECTS MED, V29, P407, DOI 10.1016-j.mam.2008.07.002; Crabtree NJ, 2004, BONE, V35, P965, DOI 10.1016-j.bone.2004.06.009; Daly Robin M, 2007, Med Sport Sci, V51, P33; Deere K, 2012, J BONE MINER RES, V27, P1887, DOI 10.1002-jbmr.1631; DiVasta AD, 2007, OSTEOPOROSIS INT, V18, P797, DOI 10.1007-s00198-006-0308-6; DOYLE F, 1970, LANCET, V1, P391; Ducher G, 2005, BONE, V37, P457, DOI 10.1016-j.bone.2005.05.014; El Hajj Fuleihan G, 2007, 6 INT S NUTR ASP OST; El Hage R, 2010, J BONE MINER METAB, V28, P595, DOI 10.1007-s00774-010-0176-1; Ferry B, 2013, JOINT BONE SPINE, V80, P57, DOI 10.1016-j.jbspin.2012.01.006; Ferry B, 2011, J BONE MINER METAB, V29, P342, DOI 10.1007-s00774-010-0226-8; Forwood MR, 2004, BONE, V35, P973, DOI 10.1016-j.bone.2004.06.005; Forwood MR, 2006, BONE, V38, P576, DOI 10.1016-j.bone.2005.09.021; FULEIHAN GE, 2007, INT C SERIES, V1297, P91; Fuleihan GE, 2006, J CLIN ENDOCR METAB, V91, P405, DOI 10.1210-jc.2005-1436; Fulton J P, 1999, Med Health R I, V82, P110; GLASTRE C, 1990, J CLIN ENDOCR METAB, V70, P1330; Heaney RP, 2000, OSTEOPOROSIS INT, V11, P985, DOI 10.1007-s001980070020; Hind K, 2007, BONE, V40, P14, DOI 10.1016-j.bone.2006.07.006; Holick MF, 2007, NEW ENGL J MED, V357, P266, DOI 10.1056-NEJMra070553; Jackowski SA, 2011, J BONE MINER RES, V26, P2753, DOI 10.1002-jbmr.468; Jackowski SA, 2009, BONE, V44, P1186, DOI 10.1016-j.bone.2009.02.008; KRALL EA, 1993, J BONE MINER RES, V8, P1; Lawson EA, 2010, BONE, V46, P458, DOI 10.1016-j.bone.2009.09.005; MacDonald H, 2006, BONE, V39, P598, DOI 10.1016-j.bone.2006.02.057; Maimoun L, 2011, OSTEOPOROSIS INT, V22, P3055, DOI 10.1007-s00198-011-1541-1; MARTIN RB, 1984, J BIOMECH, V17, P195, DOI 10.1016-0021-9290(84)90010-1; Nabulsi M, 2013, J CLIN DENSITOM, V16, P223, DOI 10.1016-j.jocd.2012.04.004; Ondrak KS, 2007, SPORTS MED, V37, P587, DOI 10.2165-00007256-200737070-00003; Petit MA, 2005, BONE, V36, P568, DOI 10.1016-j.bone.2004.12.003; Petit MA, 2004, BONE, V35, P750, DOI 10.1016-j.bone.2004.05.008; Petit MA, 2002, J BONE MINER RES, V17, P363, DOI 10.1359-jbmr.2002.17.3.363; Rauch F, 2004, BONE, V34, P771, DOI 10.1016-j.bone.2004.01.022; Rittweger J, 2000, BONE, V27, P319, DOI 10.1016-S8756-3282(00)00327-6; Rizzoli R, 2010, BONE, V46, P294, DOI 10.1016-j.bone.2009.10.005; Runyan SM, 2003, J AM DIET ASSOC, V103, P1320, DOI [10.1016-S0002-8223(03)01075-7, 10.1053-S0002-8223(03)01075-7]; Sayers A, 2012, OSTEOPOROSIS INT, V23, P2117, DOI 10.1007-s00198-011-1813-9; Schoenau E, 2002, J BONE MINER RES, V17, P1095, DOI 10.1359-jbmr.2002.17.6.1095; Semanick LM, 2005, CALCIFIED TISSUE INT, V77, P160, DOI 10.1007-s00223-005-0037-4; Stoffman N, 2009, CURR OPIN PEDIATR, V21, P465, DOI 10.1097-MOP.0b013e32832da096; Tanner JM, 1978, TXB PAEDIAT, V1, P249; Tournis S, 2010, J CLIN ENDOCR METAB, V95, P2755, DOI 10.1210-jc.2009-2382; Viljakainen HT, 2006, J BONE MINER RES, V21, P836, DOI 10.1359-JBMR.060302; Ward KA, 2010, J CLIN ENDOCR METAB, V95, P4643, DOI 10.1210-jc.2009-2725; Winzenberg T, 2011, BRIT MED J, V342, DOI 10.1136-bmj.c7254; YOSHIKAWA S, 1979, ENDOCRINOL JAPON, V26, P6533
Ultrasonography of salivary glands in primary Sjogren's syndrome: a comparison with contrast sialography and scintigraphy
No full textUltrasonography of salivary glands in primary Sjogren's syndrome: a comparison with contrast sialography and scintigraphy Author(s): Salaffi, F (Salaffi, F.)1; Carotti, M (Carotti, M.)2; Iagnocco, A (Iagnocco, A.)3; Luccioli, F (Luccioli, F.)4; Ramonda, R (Ramonda, R.)5; Sabatini, E (Sabatini, E.)3; De Nicola, M (De Nicola, M.)6; Maggi, M (Maggi, M.)6; Priori, R (Priori, R.)3; Valesini, G (Valesini, G.)3; Gerli, R (Gerli, R.)4; Punzi, L (Punzi, L.)5; Giuseppetti, GM (Giuseppetti, G. M.)2; Salvolini, U (Salvolini, U.)6; Grassi, W (Grassi, W.)1 Source:
RHEUMATOLOGY Volume: 47 Issue: 8 Pages: 1244-1249
DOI: 0.1093/rheumatology/ken222 Published: AUG 2008 Times Cited: 10 (from Web of Science) Cited References: 40 [ view related records ] Citation Map Abstract: Objective. To compare ultrasonography (US) of salivary glands with contrast sialography and scintigraphy, in order to evaluate the diagnostic value of this method in primary SS (pSS).
Methods. The diagnostic value of parotid gland US was studied in 77 patients with pSS (male/female ratio 3/74; mean age 54 yrs) and in 79 with sicca symptoms but without SS. The two groups were matched for sex and age. Imaging findings of US were graded using an ultrasonographic score ranging from 0 to 16, which was obtained by the sum of the scores for each parotid and submandibular gland. The sialographic and scintigraphic patterns were classified in four different stages. The area under receiver operating characteristic curve (AUC-ROC) was employed to evaluate the screening methods performance.
Results. Of the 77 patients with pSS, 66 had abnormal US findings. Mean US score in pSS patients was 9.0 (range from 3 to 16). Subjects without confirmed pSS had the mean US score 3.9 (range from 0 to 9) (P < 0.0001). Results of sialography showed that 59 pSS patients had abnormal findings at Stage 1 (n = 4), Stage 2 (n = 8), Stage 3 (n = 33) or Stage 4 (n = 14), and 58 patients had abnormal scintigraphic findings at Stage 1 (n = 11), Stage 2 (n = 18), Stage 3 (n = 25) or Stage 4 (n = 4). Through ROC curves US arose as the best performer (AUC = 0.863 +/- 0.030), followed by sialography (AUC = 0.804 +/- 0.035) and by salivary gland scintigraphy (AUC = 0.783 +/- 0.037). The difference between AUC-ROC curve of salivary gland US and scintigraphy was significant (P = 0.034). Setting the cut-off score 6 US resulted in the best ratio of sensitivity (75.3%) to specificity (83.5%), with a likelihood ratio of 4.58. If a threshold 8.0 was applied the test gained specificity, at the cost of a serious loss of sensitivity (sensitivity 54.5%, specificity 97.5%, likelihood ratio 21.5).
Conclusions. Salivary gland US is a useful method in visualizing glandular structural changes in patients suspected of having pSS and it may represent a good option as a first-line imaging tool in the diagnostics of the disease. Accession Number: WOS:000257787200026 Document Type: Article Language: English Author Keywords: Sjogren's syndrome; salivary glands; ultrasonography; sialography; salivary gland scintigraphy; diagnosis KeyWords Plus: COLOR DOPPLER SONOGRAPHY; PAROTID SIALOGRAPHY; CLASSIFICATION CRITERIA; DIAGNOSTIC-CRITERIA; SICCA SYNDROME; BIOPSY; ECHOGRAPHY Reprint Address: Salaffi, F (reprint author), Univ Politecn Marche, Cattedra Reumatol, Via Colli 52, Ancona, Italy Addresses:
1. Polytechn Univ Marche Reg, Dept Rheumatol, Ancona, Italy
2. Polytechn Univ Marche Reg, Dept Radiol, Ancona, Italy
3. Univ Rome, Rheumatol Unit Sapienza, Rome, Italy
4. Univ Perugia, Dept Clin & Expt Med, Rheumatol Unit, I-06100 Perugia, Italy
5. Univ Padua, Dept Clin & Expt Med, Rheumatol Unit, Padua, Italy
6. Polytechn Univ Marche Reg, Dept Neuroradiol, Ancona, Italy E-mail Address: [email protected] Publisher: OXFORD UNIV PRESS, GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND Web of Science Category: Rheumatology Subject Area: Rheumatology IDS Number: 328GU ISSN: 1462-032
Short- and long-term safety of weekly high-dose vitamin D3 supplementation in school children
No full textBackground: Hypovitaminosis D is prevalent in youth worldwide, but the safety of vitamin D at doses exceeding 200 IU-d is unknown in this age group. We assessed the safety of high doses of vitamin D3 administered to apparently healthy schoolchildren. Methods: To assess short-term safety, 25 subjects randomly received placebo or vitamin D3 at doses of 14,000 IU-wk for 8 wk. To assess long-term safety, 340 subjects randomly received placebo, vitamin D3 as 1,400 IU-wk or 14,000 IU-wk for 1 yr. Biochemical variables were monitored at 0, 2, 4, 6, and 8 wk and 8 wk off therapy in the short-term study and at 0, 6, and 12 months in the long-term study. Results: In both the short- and long-term studies, mean serum calcium and 1,25-hydroxyvitamin levels did not change in any group. In the short-term study, mean 25-hydroxyvitamin concentrations increased from 44 (± 11) to 54 (± 19) ng-ml in the treated groups (P = 0.033). In the long-term study, mean 25-hydroxyvitamin D levels increased from 15 ± 8 to 19 ± 7 ng-ml (P andlt; 0.0001) in subjects receiving 1,400 IU-wk and from 15 ± 7 to 36 ± 22 ng-ml (P andlt; 0.0001) in the group receiving 14,000 IU-wk. No subject developed vitamin D intoxication. Conclusion: Vitamin D 3 at doses equivalent to 2000 IU-d for 1 yr is safe in adolescents and results in desirable vitamin D levels. Copyright © 2008 by The Endocrine Society.AKSNES L, 1982, J CLIN ENDOCR METAB, V55, P94; Armas LAG, 2004, J CLIN ENDOCR METAB, V89, P5387, DOI 10.1210-jc.2004-0360; Binkley N, 2004, J CLIN ENDOCR METAB, V89, P3152, DOI 10.1210-jc.2003-031979; Chel V, 2008, OSTEOPOROSIS INT, V19, P663, DOI 10.1007-s00198-007-0465-2; *COMM SCI EV DIET, 1997, DIET REF INT CAL PHO; *COMM SCI EV DIET, 1999, DIET REF INT CALC PH; Baker SS, 1999, PEDIATRICS, V104, P1152; Dahifar Hossein, 2006, J Med Invest, V53, P204, DOI 10.2152-jmi.53.204; Dawson-Hughes B, 2005, OSTEOPOROSIS INT, V16, P713, DOI 10.1007-s00198-005-1867-7; Docio S, 1998, J BONE MINER RES, V13, P544, DOI 10.1359-jbmr.1998.13.4.544; El-Hajj Fuleihan G, 2001, PEDIATRICS, V107, P1; Fuleihan GE, 2006, J CLIN ENDOCR METAB, V91, P405, DOI 10.1210-jc.2005-1436; FULEIHAN GEH, 2007, NUTR ASPECTS OSTEOPO, V1297, P91; Gartner LM, 2003, PEDIATRICS, V111, P908, DOI 10.1542-peds.111.4.908; GLASTRE C, 1990, J CLIN ENDOCR METAB, V70, P1330; Gordon CM, 2004, ARCH PEDIAT ADOL MED, V158, P531, DOI 10.1001-archpedi.158.6.531; Guillemant J, 1999, OSTEOPOROSIS INT, V10, P222, DOI 10.1007-s001980050219; Guillemant J, 1995, BONE, V17, P513, DOI 10.1016-8756-3282(95)00401-7; Guillemant J, 2001, OSTEOPOROSIS INT, V12, P875, DOI 10.1007-s001980170040; Hathcock JN, 2007, AM J CLIN NUTR, V85, P6; Heaney RP, 2003, AM J CLIN NUTR, V78, P912; Holick MF, 2007, NEW ENGL J MED, V357, P266, DOI 10.1056-NEJMra070553; Holick MF, 2006, MAYO CLIN PROC, V81, P353; Hollis BW, 2004, J CLIN ENDOCR METAB, V89, P3149, DOI 10.1210-jc.2004-0682; Houghton LA, 2006, AM J CLIN NUTR, V84, P694; ILICH JZ, 1997, CALCIFIED TISSUE INT, P61104; Knight JA, 2007, CANCER EPIDEM BIOMAR, V16, P422, DOI 10.1158-1055-9965.EPI-06-0865; Lips P, 1999, OSTEOPOROSIS INT, V9, P394, DOI 10.1007-s001980050162; Lips P, 2004, J STEROID BIOCHEM, V89-90, P611, DOI 10.1016-j.jsbmb.2004.03.040; LOCKITCH G, 1988, CLIN CHEM, V34, P1622; Luscombe CJ, 2001, LANCET, V358, P641, DOI 10.1016-S0140-6736(01)05788-9; MAALOUF J, 2005, BONE S1, V36, pS50; Maalouf J, 2006, J BONE MINER RES, V21, pS29; Matkovic Velimir, 2005, American Journal of Clinical Nutrition, V81, P175; Oliveri B, 1996, EUR J CLIN NUTR, V50, P807; OLIVERI MB, 1993, BONE MINER, V20, P99, DOI 10.1016-S0169-6009(08)80041-4; Pittas AG, 2006, DIABETES CARE, V29, P650, DOI 10.2337-diacare.29.03.06.dc05-1961; Trang HM, 1998, AM J CLIN NUTR, V68, P854; VIETH R, 1990, AM J PHYSIOL, V258, pE780; Vieth R, 1999, AM J CLIN NUTR, V69, P842; Vieth Reinhold, 2004, Nutr J, V3, P8, DOI 10.1186-1475-2891-3-8; Vieth R, 2001, AM J CLIN NUTR, V73, P288; Vieth R, 2004, J STEROID BIOCHEM, V89-90, P575, DOI 10.1016-j.jsbmb.2004.03.038; Vieth R, 2007, AM J CLIN NUTR, V85, P649; Viljakainen HT, 2006, J BONE MINER RES, V21, P836, DOI 10.1359-JBMR.060302; Weaver CM, 1999, J CLIN ENDOCR METAB, V84, P1839, DOI 10.1210-jc.84.6.183962545
Age but not gender modulates the relationship between PTH and vitamin D
No full textContext: It is unclear whether the relationship between 25-OHD and PTH is modulated by age or gender. Objective: To assess the 25-OHD-PTH relationship in 340 adolescents (10-17. years) and 443 elderly (65-85. years) of the same ethnic group, and living in the same sunny country. Assessments: Calcium intake was estimated. Serum calcium, phosphorus, 25-OHD and PTH were measured. Body fat was determined by DXA. Results: 25-OHD levels were lower in the elderly in the overall group (p 0.001) and within genders. 25-OHD levels were lower in females in the overall group and within age subgroups (p 0.05). PTH levels were higher in the elderly in the overall population and in both genders (p 0.001). There were no gender differences in PTH levels within age subgroups. For the same 25-OHD level, PTH levels were comparable across genders but were 1.5-2 folds higher in the elderly compared to adolescents (p 0.001). PTH correlated positively with age (p 0.001), body fat (p= 0.02), and negatively with calcium intake (p 0.001), and 25-OHD (p 0.001). The magnitude of the correlation with 25-OHD decreased after adjustment for age but not for gender. In multivariate analyses, age, 25-OHD and fat mass were independent predictors for PTH. In the elderly, after adjustment for serum creatinine, only 25-OHD and creatinine were independent predictors of PTH. Conclusion: The negative relationship between 25-OHD and PTH is modulated by age but not gender. Desirable 25-OHD levels derived from examining the 25-OHD-PTH relationship should therefore take into account the age of the population of interest. © 2010 Elsevier Inc.Abrams SA, 2005, J CLIN ENDOCR METAB, V90, P5576, DOI 10.1210-jc.2005-1021; Adami S, 2008, BONE, V42, P267, DOI 10.1016-j.bone.2007.10.003; Aloia JF, 2006, AM J CLIN NUTR, V84, P602; Arabi A, 2006, BONE, V39, P268, DOI 10.1016-j.bone.2006.01.140; ARABI A, J BONE MINER RES S1, V23, pM179; Atli T, 2005, ARCH GERONTOL GERIAT, V40, P53, DOI 10.1016-j.archger.2004.05.006; Benjamin A, 2009, OSTEOPOROSIS INT, V20, P1795, DOI 10.1007-s00198-009-0873-6; Bolland MJ, 2006, BONE, V38, P317, DOI 10.1016-j.bone.2005.08.018; Bonofiglio D, 2000, BRIT J NUTR, V84, P111; Bonofiglio D, 2001, HORM METAB RES, V33, P170, DOI 10.1055-s-2001-14931; Carnevale V, 2001, OSTEOPOROSIS INT, V12, P1026, DOI 10.1007-s001980170012; Dawson-Hughes B, 2005, OSTEOPOROSIS INT, V16, P713, DOI 10.1007-s00198-005-1867-7; Fuleihan GEH, 2001, PEDIATRICS, V107, DOI 10.1542-peds.107.4.e53; Fuleihan GE, 2006, J CLIN ENDOCR METAB, V91, P405, DOI 10.1210-jc.2005-1436; Grant WB, 2005, ALTERN MED REV, V10, P94; GREY AB, 1994, ANN INTERN MED, V121, P745; GUNNARSSON O, 2008, J INT MED, V265, P488; Haarburger D, 2009, J CLIN PATHOL, V62, P567, DOI 10.1136-jcp.2008.062877; Hagenau T, 2009, OSTEOPOROSIS INT, V20, P133, DOI 10.1007-s00198-008-0626-y; Harris SS, 2007, J CLIN ENDOCR METAB, V92, P3155, DOI 10.1210-jc.2007-0722; Hill TR, 2010, OSTEOPOROSIS INT, V21, P695, DOI 10.1007-s00198-009-0959-1; HOLICK M, 2009, NEW ENGL J MED, V19, P266; Khosla S, 1997, J CLIN ENDOCR METAB, V82, P1522, DOI 10.1210-jc.82.5.1522; Kuchuk NO, 2009, J CLIN ENDOCR METAB, V94, P1244, DOI 10.1210-jc.2008-1832; Kull M, 2009, INTERN MED J, V39, P256, DOI 10.1111-j.1445-5994.2009.01900.x; Lagunova Z, 2009, ANTICANCER RES, V29, P3713; Lamberg-Allardt CJE, 2001, J BONE MINER RES, V16, P2066, DOI 10.1359-jbmr.2001.16.11.2066; Li J, 2008, J STEROID BIOCHEM, V112, P122, DOI 10.1016-j.jsbmb.2008.09.006; MACLAUGHLIN J, 1985, J CLIN INVEST, V76, P1536, DOI 10.1172-JCI112134; Maggio D, 2005, J GERONTOL A-BIOL, V60, P1414; Mithal A, 2009, OSTEOPOROSIS INT, V20, P1807, DOI 10.1007-s00198-009-0954-6; Nordin BEC, 2004, AM J CLIN NUTR, V80, P998; Patel S, 2007, CALCIFIED TISSUE INT, V80, P221, DOI 10.1007-s00223-007-9001-9; Plotnikoff GA, 2003, MAYO CLIN PROC, V78, P1463; QUESADA JM, 1992, J CLIN ENDOCR METAB, V75, P494, DOI 10.1210-jc.75.2.494; Reis JP, 2007, DIABETES CARE, V30, P1549, DOI 10.2337-dc06-2438; REJNMARK L, 2008, J BONE MINER RES S1, V24; Salamoun MM, 2005, EUR J CLIN NUTR, V59, P177, DOI 10.1038-sj.ejcn.1602056; Snijder MB, 2005, J CLIN ENDOCR METAB, V90, P4119, DOI 10.1210-jc.2005-0216; Steingrimsdottir L, 2005, JAMA-J AM MED ASSOC, V294, P2336, DOI 10.1001-jama.294.18.2336; Tylavsky FA, 2007, J AM COLL NUTR, V26, P462; Valina-Toth ALB, 2010, CLIN ENDOCRINOL, V72, P595, DOI 10.1111-j.1365-2265.2009.03676.x; Vieth R, 2003, J CLIN ENDOCR METAB, V88, P185, DOI 10.1210-jc.2002-021064; Weaver CM, 2008, J CLIN ENDOCR METAB, V93, P3907, DOI 10.1210-jc.2008-0645; Yan L, 2003, BONE, V33, P620, DOI 10.1016-S8756-3282(03)00216-3; Young KA, 2009, J CLIN ENDOCR METAB, V94, P3306, DOI 10.1210-jc.2009-007917151
Modeling Pathways for Low Bone Mass in Children With Malignancies
No full textChildren with malignancies have low bone mass. Pathways for metabolic bone disease were investigated in children with cancer by concomitantly assessing lifestyle, clinical, and biochemical predictors of bone mass. Forty-one children who were receiving cancer therapy for 61 weeks and 39 controls were studied. Data on lifestyle factors, biochemical and hormonal parameters, dual-energy X-ray absorptiometry bone mass measurements, body composition, and bone age were obtained. Compared with controls, patients had higher weight percentile and fat mass, a 6-month delay in bone age, and lower estradiol levels. They also had higher parathyroid hormone levels and lower bone remodeling markers and bone mass. Age, height, lean mass, fat mass, and bone maturation correlated positively with several bone mass variables, so did serum estradiol, testosterone, and markers of bone remodeling. Conversely, corticosteroids, methotrexate (MTX), and intrathecal therapy negatively correlated with bone mass at the spine and hip (R = -0.33 to 0.40, p 0.04). In the adjusted analyses, bone maturation, serum osteocalcin level, MTX, and intrathecal therapy were significant predictors of lumbar spine and total body Z-scores, bone maturation accounting for the largest proportion in Z-score variance. Chemotherapy-induced delay in bone maturation and suppression of bone modeling are major pathophysiologic pathways predicting bone mass in children with malignancies. © 2009 The International Society for Clinical Densitometry.Arabi A, 2004, AM J CLIN NUTR, V80, P1428; Arikoski P, 1999, ARCH DIS CHILD, V80, P143; Arikoski P, 1999, J CLIN ENDOCR METAB, V84, P3174, DOI 10.1210-jc.84.9.3174; Arikoski P, 1999, MED PEDIATR ONCOL, V33, P455, DOI 10.1002-(SICI)1096-911X(199911)33:5455::AID-MPO43.0.CO;2-3; Arikoski P, 1999, J BONE MINER RES, V14, P2002, DOI 10.1359-jbmr.1999.14.12.2002; Bak M, 2006, PEDIATR NEPHROL, V21, P350, DOI 10.1007-s00467-005-2118-z; Boot AM, 1999, EUR J CANCER, V35, P1693, DOI 10.1016-S0959-8049(99)00143-4; Canalis E, 2007, OSTEOPOROSIS INT, V18, P1319, DOI 10.1007-s00198-007-0394-0; Chemaitilly W, 2006, J CLIN ENDOCR METAB, V91, P1723, DOI 10.1210-jc.2006-0020; Cicognani A, 2003, J PEDIATR ENDOCR MET, V16, P321; Dawson-Hughes B, 2005, OSTEOPOROSIS INT, V16, P713, DOI 10.1007-s00198-005-1867-7; El-Hajj Fuleihan G, 2001, PEDIATRICS, V107, P1; FLEMING KH, 1994, J NUTR, V124, pS1426; FULEIHAN GE, 2007, INT C SERIES, V1297, P91; FULEIHAN GE, 2008, 35 ANN M AM SOC BON; Fuleihan GE, 2006, J CLIN ENDOCR METAB, V91, P405, DOI 10.1210-jc.2005-1436; Gordon CM, 2008, J CLIN DENSITOM, V11, P43, DOI 10.1016-j.jocd.2007.12.005; Holick MF, 2007, NEW ENGL J MED, V357, P266, DOI 10.1056-NEJMra070553; Hoorweg-Nijman JJG, 1999, CLIN ENDOCRINOL, V50, P237, DOI 10.1046-j.1365-2265.1999.00654.x; Kadan-Lottick N, 2001, J PEDIATR, V138, P898, DOI 10.1067-mpd.2001.113102; KATZMAN DK, 1991, J CLIN ENDOCR METAB, V73, P1332; Mackie EJ, 1996, MED PEDIATR ONCOL, V27, P74, DOI 10.1002-(SICI)1096-911X(199608)27:274::AID-MPO23.0.CO;2-Q; Mandel K, 2004, J CLIN ONCOL, V22, P1215, DOI 10.1200-JCO.2004.04.199; Mulder JE, 2004, J CLIN DENSITOM, V7, P432, DOI 10.1385-JCD:7:4:432; Murphy AJ, 2006, AM J CLIN NUTR, V83, P70; Nysom K, 2001, MED PEDIATR ONCOL, V37, P518, DOI 10.1002-mpo.1245; Pagano-Therrien Jesica, 2005, J Pediatr Oncol Nurs, V22, P328, DOI 10.1177-1043454205281760; Pui C.-H., 2004, Annals of Hematology, V83, pS124; Pui CH, 2006, NEW ENGL J MED, V354, P166, DOI 10.1056-NEJMra052603; Salamoun MM, 2005, EUR J CLIN NUTR, V59, P177, DOI 10.1038-sj.ejcn.1602056; Tanner JM, 1978, TXB PAEDIAT, V1, P249; Tillmann V, 2002, J BONE MINER RES, V17, P1073, DOI 10.1359-jbmr.2002.17.6.1073; van der Sluis IM, 2002, J PEDIATR, V141, P204, DOI 10.1067-mpd.2002.125728; Wasilewski-Masker K, 2008, PEDIATRICS, V121, pE705, DOI 10.1542-peds.2007-1396; Zemel BS, 2007, PEDIATR RES, V61, P607, DOI 10.1203-pdr.0b013e318045bdca; Zhao LJ, 2008, J BONE MINER RES, V23, P17, DOI 10.1359-JBMR.07081344
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